Alcoholic neuropathy: possible mechanisms and future treatment possibilities PMC

Overcoming alcohol use may not reverse the damage that has been done, but it can prevent nerve damage and other health issues from getting worse. Getting help as quickly as possible can also reduce the alcoholic neuropathy recovery time, which can vary based on the extent of a person’s nerve damage and other factors. The signs and symptoms of alcoholic neuropathy can vary based on the person, their medical history, and the https://ecosoberhouse.com/ bodily functions most impacted by their alcohol use. But if you have developed neuropathy as a result of alcohol use, it’s important to stop drinking as soon as possible. Professional and peer help through programs such as Alcoholics Anonymous or other substance abuse programs can help you reduce your alcohol consumption. Talk to your healthcare provider about the best treatment plan to start on your road to recovery.

Others may be able to stop drinking with outpatient therapy or social support. However, it is most common among people with a history of heavy, long-term alcohol use. Some of the most common symptoms are numbness or tingling sensation of the extremities, pain or a burning sensation in the extremities, difficulty walking, difficulty urinating, and difficulty talking or swallowing. Knowing how much alcohol can cause neuropathy and how to handle the condition if you start to experience its symptoms is crucial if you consume alcohol.

Alcohol depletes the pool of liver proteins

One of the other important issues in alcoholic individuals is the source of their calorie intake. These individuals draw the majority of calories from calorie rich alcoholic beverages with low nutritive value. Chronic abuse of alcohol depletes the pool of liver proteins which are consumed for energy production and insufficient intake of proteins only worsens this imbalance. Resulting disturbances in protein and lipid metabolism lead to undernourishment which adversely influences other metabolic pathways, including those influencing the function of the nervous system. Studies on this condition have estimated that up to 66 percent of chronic alcoholics develop permanent nerve damage as a result of their drinking.

• This can be achieved by complete alcohol abstinence and a balanced diet primarily supplemented by B6, B12, and E vitamins, as well as folate, thiamine, and niacin.
• Nerve damage that is caused by or related to alcohol use is known as alcoholic neuropathy, or polyneuropathy when multiple nerves are affected.
• Current postulation holds that dysfunctions within the central and peripheral nervous system are due to both direct and indirect toxic effects of alcohol [31, 85,86,87].
• The lack of thiamine in the nervous system affects the cellular structure and can cause cell membrane damage and irregular ectopic cells.
• Also, levels of alcohol in the blood higher than 60 mg/dL confirmed the consistency of this protocol and were compatible with other studies (Bell et al., 2006, Simms et al., 2008a, Simms et al., 2008b).

Regarding the other parameters, lacrimation, pupil reflex, palpebral closure, salivation and breathing, there was no significant difference between animals. In both groups AL and CO, the animals showed absence of salivation and lacrimation, normal breathing and palpebral closure, and pupil size with myosis (Table 2). Right before the beginning of the perfusion, 0.5 ml of blood from the left ventricle was collected. The samples were alcohol neuropathy placed into heparinized tubes and centrifuged at 2300 rpm, 4 ºC for 15 min (Biochain, Newark, CA, USA). Blood alcohol concentration analysis was performed by the method of spectrophotometry with the enzyme kit for the enzyme NAD-ADH (Conte et al., 2019a, Conte et al., 2019b, Wscieklica et al., 2019). Peripheral neuropathy can result from traumatic injuries, infections, metabolic problems, inherited causes and exposure to toxins.

Mean thickness of myelin sheath (tmyelin)

This information would lead to a more accurate classification of ALN based on its etiology. The primary goal of this article is to review the evidence of proposed mechanisms in the development of ALN, specifically those related to thiamine deficiency and ethanol. Chronic alcohol consumption leads to malnutrition with dysfunctions in protein and lipid metabolism which affect the metabolic pathways and progression of ALN symptoms within the central and peripheral nervous systems [89]. The direct toxic effects of alcohol and its metabolites (mainly acetaldehyde) are crucial in ALN etiology [64]. It has been demonstrated that incubation of neural cells with advanced glycation end products of acetaldehyde (AA-AGE) induced dose-dependent degradation of neuronal cells while the addition of AA-AGE antibodies reduced neurotoxicity [51, 90]. Other findings showed that decreased activity of aldehyde dehydrogenase leads to peripheral neuropathy [76, 91].

Patients with small fiber neuropathy commonly report burning pain and may tell you, “My feet burn.” Patients may be hypersensitive to a stimulus (hyperesthesia). Patients may also experience numbness, restless legs syndrome, dry eyes and mouth, increased sweating, stomach problems, bladder control issues, skin discoloration, and cardiovascular symptoms. Nerve degeneration progresses from sensory symptoms to include motor function problems of the lower and upper extremities.

THE THIAMINE STORY

Appenzeller and Ogin (1974) showed that alcohol-dependent and diabetic patients had a reduced number of large fibers (greater than 5 μm) and greater density of autonomic fibers (possibly because of the degeneration followed by a partial regeneration) [161]. The reduction of internodal length contributes to the decreased speed of nerve conduction which may be implemented in impairments in perspiration, baroreceptor reflexes, and functions of internal organs. To determine the functions of the sympathetic division of the autonomic nervous system (ANS), sympathetic skin response (SSR) is used; the abnormal results of this test suggest subclinical transmission impairments [162]. Navarro et al. (1993) showed that nearly half of the alcohol-dependent patients without AAN symptoms and any aberrations in electrophysiologic studies presented abnormal SSR results [163]. In a similar study, SSR was used to assess the number of reactive sweat glands (SGN), which turned out to be decreased in alcohol-dependent patients [164].